Metabolic stress‐dependent regulation of the mitochondrial biogenic molecular response to high‐intensity exercise in human skeletal muscle

Fiorenza, Matteo; Gunnarsson, Thomas P.; Hostrup, Morten; Iaia, F. Marcello; Schena, Federico; Pilegaard, Henriette; Bangsbo, Jens

doi:10.1113/jp275972

Cited by 94 publications

(103 citation statements)

References 89 publications

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“…For example, a single bout of exercise induces a rapid increase of PGC‐1α protein content in human skeletal muscle (29). Moreover, PGC‐1α translocation to the nucleus (17) and estrogen‐related receptor (ERR)‐α expression occur within 2 h (16). Notably, the initial increase of peroxisome proliferator‐activated receptor‐γ coactivator (PGC)‐1α and ERR‐α transcription appears to induce the expression of MFN2 (16).…”

Section: Discussionmentioning

confidence: 99%

Human muscular mitochondrial fusion in athletes during exercise

et al. 2019

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The main objective of this work was to investigate whether mitochondrial fusion occurs in the skeletal muscle of well‐trained athletes in response to high‐intensity exercise. Well‐trained swimmers (n = 9) performed a duration‐matched sprint interval training (SIT) and high‐intensity high‐volume training (HIHVT) session on separate days. Muscle samples from triceps brachii were taken before, immediately after, and 3 h after the training sessions. Transmission electron microscopy (TEM) was applied to assess mitochondrial morphology. Moreover, expression of genes coding for regulators of mitochondrial fusion and fission were assessed by real‐time quantitative PCR. In addition, mitofusin (MFN)2 and optic atrophy 1 (OPA1) were quantified by Western blot analysis. TEM analyses showed that mitochondrial morphology remained altered for 3 h after HIHVT, whereas SIT‐induced changes were only evident immediately after exercise. Only SIT increased MFN1 and MFN2 mRNA expression, whereas SIT and HIHVT both increased MFN2 protein content 3 h after exercise. Notably, only HIHVT increased OPA1 protein content. Mitochondrial morphologic changes that suggest fusion occurs in well‐adapted athletes during exercise. However, HIHVT appears as a more robust inducer of mitochondrial fusion events than SIT. Indeed, SIT induces a rapid and transient change in mitochondrial morphology.—Huertas, J. R., Ruiz‐Ojeda, F. J., Plaza‐Díaz, J., Nordsborg, N. B., Martín‐Albo, J., Rueda‐Robles, A., Casuso, R. A. Human muscular mitochondrial fusion in athletes during exercise. FASEB J. 33, 12087‐12098 (2019). http://www.fasebj.org

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Section: Discussionmentioning

confidence: 99%

Human muscular mitochondrial fusion in athletes during exercise

et al. 2019

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“…Further, Fiorenza et al . () reported that a low‐volume sprint protocol (6 × 20 s ‘all‐out’) elicited increases in gene expression and intracellular signalling that were similar or greater than those elicited by a 50 min bout of moderate‐intensity continuous cycling involving 8 times more work. Other putative signalling events seem to occur above an intensity threshold, such as the fragmentation of the ryanodine receptor 1 protein (RYR1), which was elicited by supramaximal exercise but not lower intensity exercise (Place et al .…”

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confidence: 97%

“…We are not arguing that lower intensities of exercise are ineffective: prolonged exercise at lower intensities activates mitochondrial biogenesis, albeit perhaps in response to different intracellular signals (Fiorenza et al . ), and increases mitochondrial content (Burgomaster et al . ; Gillen et al .…”

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confidence: 99%

CrossTalk proposal: Exercise training intensity is more important than volume to promote increases in human skeletal muscle mitochondrial content

MacInnis

Skelly

Gibala

2019

The Journal of Physiology

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“…In contrast, given recent data highlighting the role of local metabolic stress in modulating acute exercise‐induced cell signaling pathways (Fiorenza et al. ), we hypothesized that the application of CWI (i.e., a systemic mediated stress) induces negligible regulatory effects on muscles that have already been subjected to the extreme local metabolic challenge of both high‐intensity exercise and low muscle glycogen availability. Confirming our hypothesis, we demonstrate that the application of post‐exercise CWI does not enhance the exercise‐induced expression of PGC‐1α mRNA in muscles that completed an acute high‐intensity cycling protocol with low (i.e., <300 mmol·kg −1 dw) or very low (i.e., <150 mmol·kg −1 dw) pre‐exercise muscle glycogen concentrations.…”

Section: Discussionmentioning

confidence: 94%

“…However, given recent data highlighting the role of local muscle metabolic stress in modulating acute exercise‐induced cell signaling pathways (Fiorenza et al. ), it is suggested that the application of CWI (i.e., a systemic mediated stress) induces negligible regulatory effects on a muscle that has already been subjected to the extreme local metabolic challenge of both high‐intensity exercise and low muscle glycogen availability.…”

Section: Introductionmentioning

confidence: 99%

Low pre‐exercise muscle glycogen availability offsets the effect of post‐exercise cold water immersion in augmenting PGC‐1α gene expression

et al. 2019

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We assessed the effects of post‐exercise cold‐water immersion (CWI) in modulating PGC‐1α mRNA expression in response to exercise commenced with low muscle glycogen availability. In a randomized repeated‐measures design, nine recreationally active males completed an acute two‐legged high‐intensity cycling protocol (8 × 5 min at 82.5% peak power output) followed by 10 min of two‐legged post‐exercise CWI (8°C) or control conditions (CON). During each trial, one limb commenced exercise with low (LOW: <300 mmol·kg −1 dw) or very low (VLOW: <150 mmol·kg −1 dw) pre‐exercise glycogen concentration, achieved via completion of a one‐legged glycogen depletion protocol undertaken the evening prior. Exercise increased ( P < 0.05) PGC‐1α mRNA at 3 h post‐exercise. Very low muscle glycogen attenuated the increase in PGC‐1α mRNA expression compared with the LOW limbs in both the control (CON VLOW ~3.6‐fold vs. CON LOW ~5.6‐fold: P = 0.023, ES 1.22 Large) and CWI conditions (CWI VLOW ~2.4‐fold vs. CWI LOW ~8.0 fold: P = 0.019, ES 1.43 Large). Furthermore, PGC‐1α mRNA expression in the CWI‐LOW trial was not significantly different to the CON LOW limb ( P = 0.281, ES 0.67 Moderate). Data demonstrate that the previously reported effects of post‐exercise CWI on PGC‐1α mRNA expression (as regulated systemically via β‐adrenergic mediated cell signaling) are offset in those conditions in which local stressors (i.e., high‐intensity exercise and low muscle glycogen availability) have already sufficiently activated the AMPK‐PGC‐1α signaling axis. Additionally, data suggest that commencing exercise with very low muscle glycogen availability attenuates PGC‐1α signaling.

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Metabolic stress‐dependent regulation of the mitochondrial biogenic molecular response to high‐intensity exercise in human skeletal muscle

Cited by 94 publications

References 89 publications

Human muscular mitochondrial fusion in athletes during exercise

Human muscular mitochondrial fusion in athletes during exercise

CrossTalk proposal: Exercise training intensity is more important than volume to promote increases in human skeletal muscle mitochondrial content

Low pre‐exercise muscle glycogen availability offsets the effect of post‐exercise cold water immersion in augmenting PGC‐1α gene expression

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